Considerable evidence has been amassed indicating that behavioral stress may constitute a major risk factor for sudden cardiac death. Until recently the prevailing view has been that psychologic influences on vulnerability were mediated mainly through a direct action of catecholamines on myocardial excitable properties. However, the possibility that alterations in coronary hemodynamic function may be involved has not been adequately explored. The proposed experimental work will be guided by the following objectives: Specific Aims: (1) To examine whether significant changes in myocardial perfusion are responsible for the enhancement of vulnerability to VF during behavioral stress in the normal and ischemic heart. (2) To determine the role of adrenergic inputs to the heart in mediating behaviorally induced changes in coronary hemodynamic function and ventricular vulnerability. (3) To define the participation of the vagus nerve in modulating the effects of behavioral stress on myocardial perfusion and susceptibility to VF. The methods to be employed will be those of coronary sinus flow thermodilution techniques, biochemical determination of coronary sinus effluent (for content of oxygen, lactate and catecholamines), and cardiac electrical testing. These investigations will serve not only to define further the underlying mechanisms mediating behaviorally induced cardiac arrhythmias, but also to evolve new clinical approaches. If for example inappropriate coronary vasoconstriction were implicated, an important clinical impact could be made since measures are now available to combat coronary artery spasm. A therapeutic strategy would thus be provided for containment of neurophysiologic precipitants of malignant arrhythmias.